Emerging Insights Into the Molecular and Cellular Basis of Glioblastoma
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Human RET Kinase Protein (His Tag)
Human RET Kinase Protein (His Tag) Catalog Number: 11997-H08H1 General Information SDS-PAGE: Gene Name Synonym: CDHF12; CDHR16; HSCR1; MEN2A; MEN2B; MTC1; PTC; RET-ELE1; RET51 Protein Construction: A DNA sequence encoding the extracellular domain of human RET (P07949-1) (Met 1-Arg 635) was fused with a polyhistidine tag at the N- terminus. Source: Human Expression Host: HEK293 Cells QC Testing Purity: > 92 % as determined by SDS-PAGE Protein Description Endotoxin: RET proto-oncogene, also known as RET, is a cell-surface molecule that < 1.0 EU per μg of the protein as determined by the LAL method transduce signals for cell growth and differentiation. It contains 1 cadherin domain and 1 protein kinase domain. RET proto-oncogene belongs to the Stability: protein kinase superfamily, tyr protein kinase family. RET proto-oncogene is involved in numerous cellular mechanisms including cell proliferation, ℃ Samples are stable for up to twelve months from date of receipt at -70 neuronal navigation, cell migration, and cell differentiation upon binding with glial cell derived neurotrophic factor family ligands. It phosphorylates Leu 29 Predicted N terminal: PTK2/FAK1 and regulates both cell death/survival balance and positional Molecular Mass: information. RET is required for the molecular mechanisms orchestration during intestine organogenesis; involved in the development of enteric The recombinant human RET consists of 618 amino acids and has a nervous system and renal organogenesis during embryonic life; promotes calculated molecular mass of 69.1 kDa. The apparent molecular mass of the formation of Peyer's patch-like structures; modulates cell adhesion via the protein is approximately 110-120 kDa in SDS-PAGE under reducing its cleavage; involved in the development of the neural crest. -
Updates on the Role of Molecular Alterations and NOTCH Signalling in the Development of Neuroendocrine Neoplasms
Journal of Clinical Medicine Review Updates on the Role of Molecular Alterations and NOTCH Signalling in the Development of Neuroendocrine Neoplasms 1,2, 1, 3, 4 Claudia von Arx y , Monica Capozzi y, Elena López-Jiménez y, Alessandro Ottaiano , Fabiana Tatangelo 5 , Annabella Di Mauro 5, Guglielmo Nasti 4, Maria Lina Tornesello 6,* and Salvatore Tafuto 1,* On behalf of ENETs (European NeuroEndocrine Tumor Society) Center of Excellence of Naples, Italy 1 Department of Abdominal Oncology, Istituto Nazionale Tumori, IRCCS Fondazione “G. Pascale”, 80131 Naples, Italy 2 Department of Surgery and Cancer, Imperial College London, London W12 0HS, UK 3 Cancer Cell Metabolism Group. Centre for Haematology, Immunology and Inflammation Department, Imperial College London, London W12 0HS, UK 4 SSD Innovative Therapies for Abdominal Metastases—Department of Abdominal Oncology, Istituto Nazionale Tumori, IRCCS—Fondazione “G. Pascale”, 80131 Naples, Italy 5 Department of Pathology, Istituto Nazionale Tumori, IRCCS—Fondazione “G. Pascale”, 80131 Naples, Italy 6 Unit of Molecular Biology and Viral Oncology, Department of Research, Istituto Nazionale Tumori IRCCS Fondazione Pascale, 80131 Naples, Italy * Correspondence: [email protected] (M.L.T.); [email protected] (S.T.) These authors contributed to this paper equally. y Received: 10 July 2019; Accepted: 20 August 2019; Published: 22 August 2019 Abstract: Neuroendocrine neoplasms (NENs) comprise a heterogeneous group of rare malignancies, mainly originating from hormone-secreting cells, which are widespread in human tissues. The identification of mutations in ATRX/DAXX genes in sporadic NENs, as well as the high burden of mutations scattered throughout the multiple endocrine neoplasia type 1 (MEN-1) gene in both sporadic and inherited syndromes, provided new insights into the molecular biology of tumour development. -
Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only. -
Delta-Like Protein 3 Prevalence in Small Cell Lung Cancer and DLL3 (SP347) Assay Characteristics
EARLY ONLINE RELEASE Note: This article was posted on the Archives Web site as an Early Online Release. Early Online Release articles have been peer reviewed, copyedited, and reviewed by the authors. Additional changes or corrections may appear in these articles when they appear in a future print issue of the Archives. Early Online Release articles are citable by using the Digital Object Identifier (DOI), a unique number given to every article. The DOI will typically appear at the end of the abstract. The DOI for this manuscript is doi: 10.5858/arpa.2018-0497-OA The final published version of this manuscript will replace the Early Online Release version at the above DOI once it is available. © 2019 College of American Pathologists Original Article Delta-like Protein 3 Prevalence in Small Cell Lung Cancer and DLL3 (SP347) Assay Characteristics Richard S. P. Huang, MD; Burton F. Holmes, PhD; Courtney Powell; Raji V. Marati, PhD; Dusty Tyree, MS; Brittany Admire, PhD; Ashley Streator; Amy E. Hanlon Newell, PhD; Javier Perez, PhD; Deepa Dalvi; Ehab A. ElGabry, MD Context.—Delta-like protein 3 (DLL3) is a protein that is Results.—Cytoplasmic and/or membranous staining was implicated in the Notch pathway. observed in 1040 of 1362 specimens of small cell lung Objective.—To present data on DLL3 prevalence in cancer (76.4%). Homogenous and/or heterogeneous and small cell lung cancer and staining characteristics of the partial and/or circumferential granular staining with varied VENTANA DLL3 (SP347) Assay. In addition, the assay’s immunoreactivity with other neoplastic and nonneoplastic intensities was noted. -
The Regulatory Roles of Phosphatases in Cancer
Oncogene (2014) 33, 939–953 & 2014 Macmillan Publishers Limited All rights reserved 0950-9232/14 www.nature.com/onc REVIEW The regulatory roles of phosphatases in cancer J Stebbing1, LC Lit1, H Zhang, RS Darrington, O Melaiu, B Rudraraju and G Giamas The relevance of potentially reversible post-translational modifications required for controlling cellular processes in cancer is one of the most thriving arenas of cellular and molecular biology. Any alteration in the balanced equilibrium between kinases and phosphatases may result in development and progression of various diseases, including different types of cancer, though phosphatases are relatively under-studied. Loss of phosphatases such as PTEN (phosphatase and tensin homologue deleted on chromosome 10), a known tumour suppressor, across tumour types lends credence to the development of phosphatidylinositol 3--kinase inhibitors alongside the use of phosphatase expression as a biomarker, though phase 3 trial data are lacking. In this review, we give an updated report on phosphatase dysregulation linked to organ-specific malignancies. Oncogene (2014) 33, 939–953; doi:10.1038/onc.2013.80; published online 18 March 2013 Keywords: cancer; phosphatases; solid tumours GASTROINTESTINAL MALIGNANCIES abs in sera were significantly associated with poor survival in Oesophageal cancer advanced ESCC, suggesting that they may have a clinical utility in Loss of PTEN (phosphatase and tensin homologue deleted on ESCC screening and diagnosis.5 chromosome 10) expression in oesophageal cancer is frequent, Cao et al.6 investigated the role of protein tyrosine phosphatase, among other gene alterations characterizing this disease. Zhou non-receptor type 12 (PTPN12) in ESCC and showed that PTPN12 et al.1 found that overexpression of PTEN suppresses growth and protein expression is higher in normal para-cancerous tissues than induces apoptosis in oesophageal cancer cell lines, through in 20 ESCC tissues. -
Role of Focal Adhesion Kinase in Small-Cell Lung Cancer and Its Potential As a Therapeutic Target
cancers Review Role of Focal Adhesion Kinase in Small-Cell Lung Cancer and Its Potential as a Therapeutic Target Frank Aboubakar Nana 1,2 , Marie Vanderputten 1 and Sebahat Ocak 1,3,* 1 Institut de Recherche Expérimentale et Clinique (IREC), Pôle de Pneumologie, ORL et Dermatologie (PNEU), Université catholique de Louvain (UCLouvain), 1200 Brussels, Belgium; [email protected] (F.A.N.); [email protected] (M.V.) 2 Division of Pneumology, Cliniques Universitaires St-Luc, UCL, 1200 Brussels, Belgium 3 Division of Pneumology, CHU UCL Namur (Godinne Site), UCL, 5530 Yvoir, Belgium * Correspondence: [email protected]; Tel.: +32-2-764-9448; Fax: +32-2-764-9440 Received: 15 September 2019; Accepted: 24 October 2019; Published: 29 October 2019 Abstract: Small-cell lung cancer (SCLC) represents 15% of all lung cancers and it is clinically the most aggressive type, being characterized by a tendency for early metastasis, with two-thirds of the patients diagnosed with an extensive stage (ES) disease and a five-year overall survival (OS) as low as 5%. There are still no effective targeted therapies in SCLC despite improved understanding of the molecular steps leading to SCLC development and progression these last years. After four decades, the only modest improvement in OS of patients suffering from ES-SCLC has recently been shown in a trial combining atezolizumab, an anti-PD-L1 immune checkpoint inhibitor, with carboplatin and etoposide, chemotherapy agents. This highlights the need to pursue research efforts in this field. Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase that is overexpressed and activated in several cancers, including SCLC, and contributing to cancer progression and metastasis through its important role in cell proliferation, survival, adhesion, spreading, migration, and invasion. -
Personalized Prediction of Acquired Resistance to EGFR-Targeted Inhibitors Using a Pathway-Based Machine Learning Approach
Cancers 2019, 11, x S1 of S9 Supplementary Materials: Personalized Prediction of Acquired Resistance to EGFR-Targeted Inhibitors Using a Pathway-Based Machine Learning Approach Young Rae Kim, Yong Wan Kim, Suh Eun Lee, Hye Won Yang and Sung Young Kim Table S1. Characteristics of individual studies. Sample Size Origin of Cancer Drug Dataset Platform S AR (Cell Lines) Lung cancer Agilent-014850 Whole Human GSE34228 26 26 (PC9) Genome Microarray 4x44K Gefitinib Epidermoid carcinoma Affymetrix Human Genome U133 GSE10696 3 3 (A431) Plus 2.0 Head and neck cancer Illumina HumanHT-12 V4.0 GSE62061 12 12 (Cal-27, SSC-25, FaDu, expression beadchip SQ20B) Erlotinib Head and neck cancer Illumina HumanHT-12 V4.0 GSE49135 3 3 (HN5) expression beadchip Lung cancer (HCC827, Illumina HumanHT-12 V3.0 GSE38310 3 6 ER3, T15-2) expression beadchip Lung cancer Illumina HumanHT-12 V3.0 GSE62504 1 2 (HCC827) expression beadchip Afatinib Lung cancer * Illumina HumanHT-12 V4.0 GSE75468 1 3 (HCC827) expression beadchip Head and neck cancer Affymetrix Human Genome U133 Cetuximab GSE21483 3 3 (SCC1) Plus 2.0 Array GEO, gene expression omnibus; GSE, gene expression series; S, sensitive; AR, acquired EGFR-TKI resistant; * Lung Cancer Cells Derived from Tumor Xenograft Model. Table S2. The performances of four penalized regression models. Model ACC precision recall F1 MCC AUROC BRIER Ridge 0.889 0.852 0.958 0.902 0.782 0.964 0.129 Lasso 0.944 0.957 0.938 0.947 0.889 0.991 0.042 Elastic Net 0.978 0.979 0.979 0.979 0.955 0.999 0.023 EPSGO Elastic Net 0.989 1.000 0.979 0.989 0.978 1.000 0.018 AUROC, area under curve of receiver operating characteristic; ACC, accuracy; MCC, Matthews correlation coefficient; EPSGO, Efficient Parameter Selection via Global Optimization algorithm. -
Pdf/Infopackage Kinex.Pdf for a Com- Domain Inhibition (15)
Protein Tyrosine Phosphatase Receptor Type γ Is a JAK Phosphatase and Negatively Regulates Leukocyte Integrin Activation This information is current as Michela Mirenda, Lara Toffali, Alessio Montresor, Giovanni of October 1, 2021. Scardoni, Claudio Sorio and Carlo Laudanna J Immunol 2015; 194:2168-2179; Prepublished online 26 January 2015; doi: 10.4049/jimmunol.1401841 http://www.jimmunol.org/content/194/5/2168 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2015/01/23/jimmunol.140184 Material 1.DCSupplemental http://www.jimmunol.org/ References This article cites 46 articles, 16 of which you can access for free at: http://www.jimmunol.org/content/194/5/2168.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on October 1, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Protein Tyrosine Phosphatase Receptor Type g Is a JAK Phosphatase and Negatively Regulates Leukocyte Integrin Activation Michela Mirenda,* Lara Toffali,*,† Alessio Montresor,*,† Giovanni Scardoni,† Claudio Sorio,* and Carlo Laudanna*,† Regulation of signal transduction networks depends on protein kinase and phosphatase activities. -
The Extracellular Matrix for Bone Regeneration
This chapter is based on human mesenchymal stromal cells in adhesion to cell-derived 5 extracellular matrix and titanium: a comparative kinome profi le analysis Marta Baroncelli1^, Gwenny M. Fuhler2^, Jeroen van de Peppel1, Willian F. Zambuzzi3, Johannes P.T.M van Leeuwen1, Bram C.J van der Eerden1°, Maikel P. Peppelenbosch2° 1Department of Internal Medicine, Erasmus MC. University Medical Center Rotterdam, Wytemaweg 80, 3015 CN, Rotterdam, The Netherlands 2Department of Gastroenterology and Hepatology, Erasmus MC, University Medical Center Rotterdam, Wytemaweg 80, 3015 CN, Rotterdam, The Netherlands 3Laboratorio de Bioensaios e Dinâmica Celular, Dep.to de Quimica e Bioquimica, Instituto de Biociências, Universidade Estadual Paulista- UNESP, Campus Botucatu, São Paulo, SP Brazil. ^, °: both authors contributed equally to this work Submitted Chapter 5 ABSTRACT The extracellular matrix (ECM) is an essential component of tissue architecture that physically supports cells and actively influences stem cell behaviour, by modulating kinase-mediated signaling cascades that are the key regulators of signal transduc- tion. Cell-derived ECMs have recently emerged in the context of bone regeneration, as they reproduce physiological tissue-architecture and ameliorate the promising properties of mesenchymal stromal cells (MSCs). Titanium scaffolds show good mechanical properties and porosity to facilitate cell adhesion, and thus have been routinely used for bone tissue engineering applications. The aim of this study was to analyze the kinomic signature of human MSCs in adhesion to an osteoblast-derived ECM that we have previously shown to be osteopromotive, and to compare it to MSCs on titanium. PamChip kinase array analysis revealed 63 phosphorylated peptides on ECM and 59 on titanium, with MSCs on ECM exhibiting significant higher levels of kinase activity than those on titanium. -
Wrangling Phosphoproteomic Data to Elucidate Cancer Signaling Pathways
University of Montana ScholarWorks at University of Montana Biological Sciences Faculty Publications Biological Sciences 1-3-2013 Wrangling Phosphoproteomic Data to Elucidate Cancer Signaling Pathways Mark L. Grimes University of Montana - Missoula, [email protected] Wan-Jui Lee Laurens van der Maaten Paul Shannon Follow this and additional works at: https://scholarworks.umt.edu/biosci_pubs Part of the Biology Commons Let us know how access to this document benefits ou.y Recommended Citation Grimes, Mark L.; Lee, Wan-Jui; van der Maaten, Laurens; and Shannon, Paul, "Wrangling Phosphoproteomic Data to Elucidate Cancer Signaling Pathways" (2013). Biological Sciences Faculty Publications. 178. https://scholarworks.umt.edu/biosci_pubs/178 This Article is brought to you for free and open access by the Biological Sciences at ScholarWorks at University of Montana. It has been accepted for inclusion in Biological Sciences Faculty Publications by an authorized administrator of ScholarWorks at University of Montana. For more information, please contact [email protected]. Wrangling Phosphoproteomic Data to Elucidate Cancer Signaling Pathways Mark L. Grimes1*, Wan-Jui Lee2, Laurens van der Maaten2, Paul Shannon3 1 Division of Biological Sciences, University of Montana, Missoula, Montana, United States of America, 2 Pattern Recognition and Bioinformatics Group, Delft University of Technology, CD Delft, The Netherlands, 3 Fred Hutchison Cancer Research Institute, Seattle, Washington, United States of America Abstract The interpretation of biological data sets is essential for generating hypotheses that guide research, yet modern methods of global analysis challenge our ability to discern meaningful patterns and then convey results in a way that can be easily appreciated. Proteomic data is especially challenging because mass spectrometry detectors often miss peptides in complex samples, resulting in sparsely populated data sets. -
And DLL4-Mediated Notch Signaling Is Essential for Adult Pancreatic Islet Homeostasis
Diabetes Volume 69, May 2020 915 DLL1- and DLL4-Mediated Notch Signaling Is Essential for Adult Pancreatic Islet Homeostasis Marina Rubey,1,2 Nirav Florian Chhabra,1,2 Daniel Gradinger,1,2 Adrián Sanz-Moreno,1 Heiko Lickert,2,3,4 Gerhard K.H. Przemeck,1,2 and Martin Hrabe de Angelis1,2,5 Diabetes 2020;69:915–926 | https://doi.org/10.2337/db19-0795 Genes of the Notch signaling pathway are expressed in with type 2 diabetes (3), sparking investigation into their different cell types and organs at different time points roles in glucose metabolism. The highly conserved D/N during embryonic development and adulthood. The Notch signaling pathway is crucial for embryonic development ligand Delta-like 1 (DLL1) controls the decision between in a wide range of different tissues (4). Although Notch ac- endocrine and exocrine fates of multipotent progenitors in tivity is required during pancreatic development (5), some the developing pancreas, and loss of Dll1 leads to pre- D/N components have also been reported to be active mature endocrine differentiation. However, the role of during adulthood. D/N signaling mediates cell-cycle regu- Delta-Notch signaling in adult tissue homeostasis is not lation via transmembrane-bound ligands (DLL1, DLL3, DLL4, ISLET STUDIES well understood. Here, we describe the spatial expression JAGGED1, and JAGGED2) and receptors (NOTCH1–4). pattern of Notch pathway components in adult murine Studies have shown that DLL1 and DLL4 regulate tissue pancreatic islets and show that DLL1 and DLL4 are renewal and maintain intestinal progenitor cells (6). Fur- specifically expressed in b-cells, whereas JAGGED1 is thermore, NOTCH/NEUROG3 signaling is active in adult expressed in a-cells. -
Examining the Role of Deltalike3 in Notch Signaling During Vertebrate Segmentation
Examining the role of Deltalike3 in Notch Signaling during Vertebrate Segmentation A Senior Honors Thesis Presented in Partial Fulfillment of the Requirements for graduation with distinction in Molecular Genetics in the undergraduate colleges of The Ohio State University by Meaghan Ebetino The Ohio State University June 2008 Project Advisor: Dr. Susan Cole, Department of Molecular Genetics 2 Table of Contents I. Introduction p. 3-22 II. Results p. 22-34 III. Discussion p. 35-39 IV. Materials and Methods p. 39-42 V. References p. 43-44 3 I. Introduction Vertebrae segmentation is an embryological process regulated in part by the Notch signaling pathway. The unperturbed temporal and spatial activities of the genes involved in the Notch signaling pathway are responsible for proper skeletal phenotypes of vertebrates. The activity of Deltalike3 (Dll3), a Notch family member has been suggested to be important in both the clock and patterning activities of the Notch signaling pathway. However, the importance of Dll3 in the clock or patterning activities of the Notch signaling for proper segmentation events to occur has not been examined. Loss of Deltalike3 expression or activity in mice results in severe vertebral abnormalities, which resemble the phenotype of mice that lack the gene Lunatic fringe (Lfng), proposed to be an inhibitor of Notch. Despite the phenotypic evidence suggesting that Dll3 is an inhibitor of Notch like Lfng, there is other conflicting data suggesting that Dll3 may act either as an inhibitor or activator of Notch. My project intends to examine the role of Dll3 as an inhibitor or activator of Notch, to determine whether the Dll3 has a more important role in the clock or patterning activities of Notch signaling, and to analyze the possibility for modifier effects between Dll3 and other Notch family members.